Restoration of mitochondria function as a target for cancer therapy

被引：83

作者：

Bhat, Tariq A. ^{[1
]}

Kumar, Sandeep ^{[1
]}

Chaudhary, Ajay K. ^{[1
]}

Yadav, Neelu ^{[1
]}

Chandra, Dhyan ^{[1
]}

机构：

[1] Roswell Pk Canc Inst, Dept Pharmacol & Therapeut, Buffalo, NY 14263 USA

来源：

DRUG DISCOVERY TODAY | 2015年 / 20卷 / 05期

基金：

美国国家卫生研究院;

关键词：

HYPOXIA-INDUCIBLE FACTOR-1-ALPHA; PYRUVATE-DEHYDROGENASE KINASE; BREAST-CANCER; GLUCOSE-METABOLISM; OXIDATIVE-PHOSPHORYLATION; DICHLOROACETATE DCA; CELL-METABOLISM; TUMOR ANGIOGENESIS; HEXOKINASE II; GROWTH-FACTOR;

D O I：

10.1016/j.drudis.2015.03.001

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

Defective oxidative phosphorylation has a crucial role in the attenuation of mitochondrial function, which confers therapy resistance in cancer. Various factors, including endogenous heat shock proteins (HSPs) and exogenous agents such as dichloroacetate, restore respiratory and other physiological functions of mitochondria in cancer cells. Functional mitochondria might ultimately lead to the restoration of apoptosis in cancer cells that are refractory to current anticancer agents. Here, we summarize the key reasons contributing to mitochondria dysfunction in cancer cells and how restoration of mitochondrial function could be exploited for cancer therapeutics.

引用

页码：635 / 643

页数：9

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